This document provides an overview of diabetes mellitus (DM), including the three main types (Type 1, Type 2, and gestational diabetes), signs and symptoms, complications, pathophysiology, oral manifestations, dental management considerations, emergency management, diagnosis, and treatment. DM is caused by either the pancreas not producing enough insulin or cells not responding properly to insulin, resulting in high blood sugar levels. The document compares and contrasts the characteristics of Type 1 and Type 2 DM.

1. SWEET
NOON TO ALL

2. DIABETES
MELLITUS

3. DR. MOHAMED ABDUL HALEEM
DEPARTMENT OF PERIODONTOLOGY AND
ORAL IMPLANTOLOGY
Universal Symbol
For Diabetes

4. CONTENTS:
 INTRODUCTION
 TYPES
 SIGN AND SYMPTOMS
 COMPLICATIONS
 PATHOPHYSIOLOGY
 ORAL MANIFESTATION AND
COMPLICATION
 DENTAL MANAGEMENT
CONSIDERATION
 EMERGENCY MANAGEMENT
 DIAGNOSIS
 TREATMENT
 REFERENCE

5. INTRODUCTION
 Diabetes mellitus (DM), is a group of metabolic
diseases in which there are high blood sugar levels over
a prolonged period.
 Symptoms of high blood sugar include frequent urination,
increased thirst, and increased hunger.

6.  If left untreated, diabetes can cause many complications.
 Acute complications can include diabetic
ketoacidosis, nonketotic hyperosmolar coma, or death.
 Serious long-term complications include heart
disease, stroke, chronic kidney failure, foot ulcers,
and damage to the eyes.

7.  Diabetes is due to either the pancreas not producing
enough insulin or the cells of the body not responding
properly to the insulin produced.
 There are three main types of diabetes mellitus:
 Type 1 DM
 Type 2 DM
 Gestational Diabetes

8.  Type 1 DM
 Results from the pancreas's failure to produce enough
insulin.
 This form was previously referred to as "insulin-
dependent diabetes mellitus" (IDDM) or "juvenile
diabetes".
 The cause is unknown.

9.  Type 2 DM
 Begins with insulin resistance, a condition in which
cells fail to respond to insulin properly.
 This form was previously referred to as "non insulin-
dependent diabetes mellitus" (NIDDM) or "adult-onset
diabetes".
 The primary cause is excessive body weight and not
enough exercise.

10. Is the third main form
and occurs in
pregnant women
without a previous
history of diabetes
Gestational Diabetes

11. COMPARISON OF TYPE 1 AND 2 DIABETES
Feature Type 1 diabetes Type 2 diabetes
Onset Sudden Gradual
Age at onset Mostly in children Mostly in adults
Body size Thin or normal Often obese
Ketoacidosis Common Rare
Autoantibodies Usually present Absent
Endogenous
insulin
Low or absent
Normal,
decreased
or increased
Concordance
in identical twins
50% 90%
Prevalence ~10% ~90%

12. SIGNS AND SYMPTOMS

13. SIGNS AND SYMPTOMS
 The classic symptoms of untreated diabetes are
 weight loss
 polyuria (increased urination)
 polydipsia (increased thirst) and
 polyphagia (increased hunger).
 Symptoms may develop rapidly (weeks or months) in
type 1 DM, while they usually develop much more slowly
and may be subtle or absent in type 2 DM.

14. In addition they also include:
 Blurry vision
 Headache
 Fatigue
 Slow healing of cuts and
 Itchy skin.
 Prolonged high blood glucose can cause glucose
absorption in the lens of the eye, which leads to changes
in its shape, resulting in vision changes.
 A number of skin rashes that can occur in diabetes are
collectively known as diabetic dermadromes
SIGNS AND SYMPTOMS

15. COMPLICATIONS
 All forms of diabetes increase the risk
of long-term complications. These
typically develop after many years
(10–20)
 The major long-term complications
relate to damage to blood vessels.
 Diabetes doubles the risk
of cardiovascular disease
 About 75% of deaths in diabetics are
due to coronary artery disease.
 Other "macrovascular"
diseases (stroke)
 peripheral vascular disease.

16. COMPLICATIONS
 The primary complications of diabetes due to damage in
small blood vessels include damage to the eyes, kidneys,
and nerves.
 Damage to the eyes, known as diabetic retinopathy, is
caused by damage to the blood vessels in the retina of
the eye, and can result in gradual vision loss
and blindness.
 Damage to the kidneys, known as diabetic nephropathy,
can lead to tissue scarring, urine protein loss, and
eventually chronic kidney disease, sometimes
requiring dialysis or kidney transplant.
 Damage to the nerves of the body, known as diabetic
neuropathy, is the most common complication of diabetes.

17. COMPLICATIONS
 The symptoms can include
numbness, tingling, pain, and altered
pain sensation, which can lead to
damage to the skin.
 Diabetes-related foot
problems (such as diabetic foot
ulcers) may occur, and can be
difficult to treat, occasionally
requiring amputation.
 Additionally, proximal diabetic
neuropathy causes painful muscle
wasting and weakness – Diabetic
Amyotrophy.

18. PATHOPHYSIOLOGY - GENERAL
 Insulin is the principal hormone that regulates the uptake
of glucose from the blood into cells of the body, especially
liver, adipose tissue and muscle, except smooth muscle, in
which insulin acts via the IGF-1 (Insulin-like growth factor -
1).
 Therefore, deficiency of insulin or the insensitivity of
its receptors plays a central role in all forms of diabetes
mellitus.

19. PATHOPHYSIOLOGY
 The body obtains glucose from
three main places:
 The intestinal absorption of food
 The breakdown of glycogen, the
storage form of glucose found in the
liver
 Gluconeogenesis, the generation of
glucose from non-carbohydrate
substrates in the body.

20. PATHOPHYSIOLOGY
Insulin plays a critical role in balancing glucose
levels in the body:
It can inhibit the breakdown of glycogen or the
process of gluconeogenesis.
It can stimulate the transport of glucose into
fat and muscle cells.
It can stimulate the storage of glucose in the
form of glycogen.

21. PATHOPHYSIOLOGY
 Insulin is released into the
blood by beta cells (β-cells),
found in the islets of
Langerhans in the pancreas, in
response to rising levels of
blood glucose, typically after
eating.
Lower glucose levels result in decreased insulin release
from the beta cells and results in the breakdown of
glycogen to glucose.
This process is mainly controlled by the
hormone glucagon, which acts in the opposite manner to
insulin.

22. PATHOPHYSIOLOGY
 If the amount of insulin available is insufficient
 If cells respond poorly to the effects of insulin
 If the insulin itself is defective
 Then glucose will not be absorbed properly by the body
cells
 The net effect is persistently high levels of blood glucose,
poor protein synthesis, and break down of fat storage
 Acidosis.

23. PATHOPHYSIOLOGY
 When the glucose concentration in the blood remains
high over time, the kidneys will reach a threshold
of reabsorption Glycosuria.
 This increases the osmotic pressure of the urine
polyuria increased fluid loss
 Lost blood volume will be replaced osmotically from
water held in body cells and other body compartments
dehydration polydipsia

24. PATHOPHYSIOLOGY - TYPE 1
 Type 1 diabetes mellitus is characterized by loss of the
insulin-producing beta cells of the islets of Langerhans in
the pancreas, leading to insulin deficiency.
 This type can be further classified as immune-mediated
or idiopathic.
 The majority of type 1 diabetes is of the immune-
mediated nature, in which a T-cell-
mediated autoimmune attack leads to the loss of beta
cells and thus insulin.

25. PATHOPHYSIOLOGY - TYPE 1
 Most affected people are otherwise healthy and of a
healthy weight when onset occurs.
 Sensitivity and responsiveness to insulin are usually
normal, especially in the early stages.
oType 1 diabetes can
affect children or adults,
but was traditionally
termed "juvenile
diabetes" because a
majority of these
diabetes cases were in
children.

26. PATHOPHYSIOLOGY - TYPE 1
 Type 1 diabetes is partly inherited, with multiple genes,
including certain HLA genotypes, known to influence the
risk of diabetes.
 In genetically susceptible people, the onset of diabetes
can be triggered by one or more environmental factors,
such as a viral infection or diet.
 Among dietary factors, gluten may lead to type 1
diabetes, but the mechanism is not fully understood

27. PATHOPHYSIOLOGY - TYPE 2
 Type 2 DM is characterized by insulin resistance.
 The defective responsiveness of body tissues to
insulin is believed to involve the insulin receptor.
 In the early stage of type 2, the predominant
abnormality is reduced insulin sensitivity.
 Type 2 DM is due primarily to lifestyle factors and
genetics.

28. PATHOPHYSIOLOGY - TYPE 2
 A number of lifestyle factors are known to be important to
the development of type 2 DM, including
 Obesity
 lack of physical activity
 poor diet
 Stress
 Dietary factors also influence the risk of developing type 2
DM such as
 sugar-sweetened drinks
 Type of fats in diet
 saturated fats and trans fatty acids increasing the risk
 polyunsaturated and monounsaturated fat decreasing the risk
 Eating lots of white rice also may increase the risk of diabetes.
 A lack of exercise is believed to cause 7% of cases

29. PATHOPHYSIOLOGY - GESTATIONAL DIABETES
 Gestational diabetes mellitus (GDM) resembles type 2 DM
in several aspects.
 Involves a combination of relatively inadequate insulin
secretion and responsiveness.
 It occurs in about 2–10% of all pregnancies and may
improve or disappear after delivery.

30. PATHOPHYSIOLOGY - GESTATIONAL DIABETES
 However, after pregnancy approximately 5–10% of
women with gestational diabetes are found to have
diabetes mellitus, most commonly type 2.
 Gestational diabetes is fully treatable, but requires
careful medical supervision throughout the
pregnancy.
 Management may include dietary changes, blood
glucose monitoring, and in some cases, insulin may
be required.

31. PATHOPHYSIOLOGY - GESTATIONAL DIABETES
 Risks to the baby include:
 Macrosomia (high birth
weight)
 Congenital Heart Defects
 Central Nervous
System Abnormalities
 Skeletal
Muscle Malformations.
oThough it may be transient, untreated
gestational diabetes can damage the health of
the fetus or mother.

32. PATHOPHYSIOLOGY - GESTATIONAL DIABETES
 A high blood bilirubin level may
result from red blood cell
destruction.
 Increased levels of insulin in a
fetus's blood may inhibit
fetal surfactant production and
cause respiratory distress
syndrome.

33. PATHOPHYSIOLOGY - GESTATIONAL DIABETES
 In severe cases, perinatal death
may occur, most commonly as a
result of poor placental perfusion
due to vascular impairment.
 Labor induction may be indicated with decreased placental
function.
 A Caesarean section may be
performed if there is marked fetal
distress or an increased risk of
injury associated with macrosomia,
such as shoulder dystocia.

34. ORAL MANIFESTATIONS AND
COMPLICATIONS
No specific oral lesions associated with diabetes. However,
there are a number of problems by presence of hyperglycemia.
 Periodontal disease:
 Microangiopathy alters antigenic challenge.
 Altered cell-mediated immune response and impaired
of neutrophil chemotaxis.
 Increased Ca+ and glucose lead to plaque formation.
 Increased collagen breakdown.

35.  Periodontal changes in seen in Diabetes Mellitus

36. ORAL MANIFESTATIONS AND
COMPLICATIONS
 Salivary glands
 Xerostomia is common, but reason is unclear.
 Tenderness, pain and burning sensation of tongue.
 May cause secondary enlargement of parotid glands with sialosis.
 Dental caries
 Increase caries prevalence in adult with diabetes. (xerostomia,
increase saliva glucose)
 Hyperglycemia state shows a positive association with dental
caries.

37. SIALOSIS
CARIOUS LESION ON
TEETH WITH XEROSTOMIA

38.  Increased risk of infection
 Reasons unknown, but macrophage metabolism
altered with inhibition of phagocytosis.
 Peripheral neuropathy and poor peripheral circulation
 Immunological deficiency
 High sugar medium
 Decrease production of Antibodies
 Candidal infection are more common and adding
effects with xerostomia
ORAL MANIFESTATIONS AND
COMPLICATIONS

39.  Delayed healing of wounds
 Due to microangiopathy and ultilisation of protein for
energy, may retard the repair of tissues.
 Increase prevalence of dry socket.
 Miscellaneous conditions
 Pulpitis : degeneration of vascular.
 Neuropathies : may affect cranial nerves. (facial)
 Drug side-effects : lichenoid reaction may be associated
with sulphonylureas (chlopropamide)
 Ulcers
ORAL MANIFESTATIONS AND
COMPLICATIONS

40. DENTAL MANAGEMENT
CONSIDERATIONS
To minimize the risk of an intraoperative emergency,
clinicians need to consider some issues before initiating
dental treatment.
 Medical history:
• Glucose levels
• Frequency of hypoglycemic episodes
• Medication, dosage and times.
• Consultation

41. DENTAL MANAGEMENT
CONSIDERATIONS
 Scheduling of visits
• Morning appointment
• Do not coincide with peak activity.
 Diet
• Ensure that the patient has eaten normally and taken
medications as usual.
 Blood glucose monitoring
• Measured before beginning. (<70 mg/dL)
 Prophylactic antibiotics
• Established infection
• Pre-operation contamination wound
• Major surgery

42. DENTAL MANAGEMENT
CONSIDERATIONS
 During treatment
• The most complication of DM occur is hypoglycemia episode.
• Hyperglycemia
 After treatment
• Infection control
• Dietary intake
• Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.

43. EMERGENCY MANAGEMENT
 Hypoglycemia
 Initial signs : mood changes, decreased spontaneity,
hunger and weakness.
 Followed by sweating, incoherence, tachycardia.
 Results in unconsciousness, hypotension,
hypothermia, seizures, coma, even death.

44. EMERGENCY MANAGEMENT
 15 grams of fast-acting oral carbohydrate.
 Measured blood sugar.
 Loss of consciousness: 25-30ml 50% dextrose solution iv.
over 3 min period.
 Glucagon 1mg.

45. EMERGENCY MANAGEMENT
 Severe hyperglycemia
 A prolonged onset
 Ketoacidosis may develop with nausea, vomiting,
abdominal pain and acetone odor.
 Difficult to different hypoglycemia or
hyperglycemia.

47. EMERGENCY MANAGEMENT
 Hyperglycemia needs medical intervention and
insulin administration.
 While emergency, give glucose first !
 Small amount is unlikely to cause significant
harm.

48. DIAGNOSIS
 Can be diagnosed by demonstrating any one of the
following:
 Fasting plasma glucose level ≥ 7.0 mmol/l (126 mg/dl)
 Plasma glucose ≥ 11.1 mmol/l (200 mg/dl) two hours
after a 75 g oral glucose load as in a glucose tolerance
test.
 Symptoms of high blood sugar and casual plasma
glucose ≥ 11.1 mmol/l (200 mg/dl)
 Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol
(≥ 6.5 DCCT %)

49. DIAGNOSIS
 Oral Glucose Tolerance Test (OGTT)
 Measures the body's ability to metobolise
glucose
 Most commonly done to check for gestational
diabetes.
 The patient is asked to take a glucose drink
and their blood glucose level is measured
before and at intervals after the sugary drink is
taken.
 For the standard glucose tolerance test, we
should drink 75 grams or 100 grams.

51. OGTT RESULT’S :
 People without diabetes
 Fasting value (before test): under 6 mmol/L
 At 2 hours: under 7.8 mmol/L
 People with impaired glucose tolerance (IGT)
 Fasting value (before test): 6.0 to 7.0 mmol/L
 At 2 hours: 7.9 to 11.0 mmol/L
 Diabetic levels
 Fasting value (before test): over 7.0 mmol/L
 At 2 hours: over 11.0 mmol/L

52. WHO DIABETES DIAGNOSTIC CRITERIA
Condition
2 Hour
Glucose
Fasting
Glucose
HbA1c
Unit
mmol/l
(mg/dl)
mmol/l
(mg/dl)
mmol/m
ol
DCCT %
Normal <7.8 (<140) <6.1 (<110) <42 <6.0
Diabetes
mellitus
≥11.1 (≥200) ≥7.0 (≥126) ≥48 ≥6.5

53. MANAGEMENT
 Lifestyle
 Good nutrition
 Regular exercise
 Diet control to maintain blood pressure.
 Medications
 Surgery
 Pancreas transplant
 kidney transplantation
 Weight loss surgery

54. REFERENCES:
 Harsh Mohan - Textbook of Pathology
 A Book Of Clinical Biochemistry-
Jay pee Brothers Medical Publishers
 Essentials of Medical Physiology
 K.D. Tripathi - Essentials of Medical Pharmacology
 Internet